Endostar enhances the radioresponse on lewis lung carcinoma by regulating HIF-1α

In order to investigate the efficacy of combining radiation therapy with endostar on Lewis lung carcinoma in mice and the interaction mechanisms of combined therapy. Tumor models were established in the hind limb of female C57 BL/6N mice by subcutaneous transplantation. The tumor-bearing mice were randomly divided into 4 groups: control group, endostar group (20 mg·kg^-1, once daily for 15 days), radiotherapy group (2 Gray per day to 10 Gray, d6-d10), and radiotherapy plus endostar group (combination group), (n=10 in each group). The tumors were applied to analysis of the tumor inhibitory rate and growth curve. Immunohistochemisty was adopted to check the expressions of microvessel density (MVD). The expression levels of Hypoxia-inducible factor 1α (HIF-1α) mRNA was tested by real-time fluorescence quantitative polymerase chain reaction (RT-PCR). The results demonstrated that the tumor inhibitory rate in combined treatment group was higher than that in other groups. Meanwhile, MVD and the level of HIF-1α mRNA were lower than that in other groups. We concluded that endostar significantly sensitized the function of radiation on Lewis lung carcinoma in mice, and this effect is working by decreasing HIF-1α, thereby increasing the killing effect of radiation on tumor cells.